Trauma, Vasc Malfrms, SAH/Aneurysms, Vein Dz, Intraparenchymal Bleeds Flashcards
Cavernous Malformation (aka cavernoma)
What is it? What can it cause?
Associated with what? What increased risk does this conjure?
What if there are multiple?
What can induce them?
CT appearance? MR appearance? CTA appearance?
- A cavernous malformation (also called a cavernoma) is a vascular hamartoma with a very small but definite bleeding risk. The clinical course of a cavernous malformation is variable and the lesion may cause seizures even in the absence of significant hemorrhage.
- Cavernous malformation is often associated with an adjacent developmental venous anomaly (DVA). There is an increased risk of bleeding if a DVA is present. However, the DVA itself does not have any bleeding risk.
- When multiple, cavernous malformations represent an inherited disorder called familial cavernomatosis.
- Cavernous malformations can be induced by radiation treatment to the brain.
- Noncontrast CT shows a well-circumscribed rounded hyperattenuating lesion. The hyperattenuation is due to microcalcification within the cavernoma__.
- MRI shows characteristic “popcorn-like” appearance of a lobular mixed signal on T1- and T2-weighted images from blood products of various ages. There is a peripheral rim of hemosiderin which is dark on GRE and T2-weighted image. There is typically no enhancement, but intense enhancement may be seen with a long delay after contrast administration. Cavernous malformations may range in size from tiny (a single focus of susceptibility artifact) to giant.
- Cavernous malformations are usually occult by vascular imaging (CTA or angiography).
Developmental Venous Anomaly
What is it?
Characteristic appearance?
Clinical management?
- A developmental venous anomaly (DVA) is an abnormal vein that provides functional venous drainage to the normal brain.
- DVA can usually only be seen on contrast-enhanced images, where it appears as a radially oriented vein with a characteristic caput medusa appearance.
- A DVA is a Do Not Touch lesion. If resected, the patient will suffer a debilitating venous infarct. The DVA must be preserved if an adjacent cavernous malformation is resected.
Capillary Telangiectasia
What is it?
Medical management?
Imaging appearance? Angiographical appearance?
- A capillary telangiectasia is an asymptomatic vascular lesion composed of dilated capillaries with interspersed normal brain.
- A capillary telangiectasia is another Do Not Touch lesion.
- Post-contrast MRI shows a faint, brush-stroke-like enhancing lesion in the brainstem or pons, without mass effect or surrounding edema. GRE may show blooming due to susceptibility.
- Similar to cavernous malformation, capillary telangiectasia is angiographically occult.
Name the high-flow and low-flow vascular malformations
- High-flow vascular malformations (i.e. with shunting):
- Arteriovenous Malformation
- Dural AV Fistula
- Low-flow vascular malformations (i.e. without shunting):
- Cavernous Malformation
- Developmental Venous Anomaly
- Capillary Telangiectasia
Arteriovenous Malformation
What is it? Where is it normally? Presentation? What kind of hemorrhage doe it usually result it?
What is the Spetzler-Martin scale?
Imaging appearance?
Does it replace or displace brain?
A bleeding AVM may be angiographically occult in what situation?
Factors that increase bleeding risk?
Treatment?
- An arteriovenous malformation (AVM) is a congenital high-flow vascular malformation consisting of directly connecting arteries and veins without an intervening capillary bed.
- AVM occurs intra-axially and 85% are supratentorial. AVM usually presents with seizures or bleeding (usually parenchymal hemorrhage, rarely subarachnoid). Aneurysms of the feeding arteries or intra-nidal arteries are often seen, which predispose to bleeding.
- The Spetzler-Martin scale helps to evaluate surgical risk for AVM resection. A large AVM draining to a deep vein in eloquent cortex is high risk, while a small AVM draining to a superficial vein in non-eloquent cortex is low risk.
- On imaging, AVM is characterized by a vascular nidus (“nest”) containing numerous serpentine vessels that appear as black flow-voids on MRI. There are usually adjacent changes to the adjacent brain including gliosis (T2 prolongation), dystrophic calcification, and blood products (blooming on T2* gradient imaging). The gliosis/encephalomalacia or mineralization seen in the adjacent brain is due to alteration in vascular flow from the AVM.
- AVM replaces rather than displaces brain. It causes minimal mass effect.
- Uncommonly, a bleeding AVM may be angiographically occult if the malformed vessels are compressed by the acute hematoma.
- Factors that increase bleeding risk that are detectable by imaging include intra-nidal aneurysm, venous ectasia, venous stenosis, deep venous drainage, and posterior fossa location.
- Treatment can be with embolization, stereotactic radiation, or surgical resection.
What is a Vein of Galen malformation?
Between what two structures?
What is the enlarged vein?
Childhood presentation?
Adult presentation?
- Vein of Galen malformation is a type of vascular malformation characterized by arteriovenous fistulae from thalamoperforator branches into the deep venous system.
- The enlarged vein is actually an enlarged median prosencephalic vein.
- In childhood, a Vein of Galen malformation is the most common extracardiac cause of high output cardiac failure. Vein of Galen malformation may also be seen in adults, but clinically would be either asymptomatic or may be the cause of Parinaud syndrome due to mass effect in the pineal region.
Dural arteriovenous fistulas
What are they?
What is the primary prognostic feature?
What is the Conard Classification?
- Dural arteriovenous fistulas are a complex group of high-flow lesions characterized by arteriovenous shunts between the meningeal arterioles and dural venules.
- The primary prognostic feature is the presence and degree of cortical venous drainage.
- The Conard classification I through IV describes lesions with progressively increased risk of bleeding. Type V is reserved for spinal dAVFs.
- Type I : No cortical venous drainage. Lowest risk of bleeding.
- Type IIA : Reflux into dural sinus but not cortical veins.
- Type IIB : Reflux into cortical veins: 10-20% hemorrhage rate.
- Type III : Direct cortical venous drainage: 40% hemorrhage rate.
- Type IV : Direct cortical venous drainage with venous ectasia: 66% hemorrhage rate.
- Type V : Spinal venous drainage. may
What spaces are can you detect acute extra-axial hemorrhage?
Is it hyperdense, isodense, or hypodense on CT?
Blood must do what before it becomes apparent on CT?
Hyperacute blood or blood in a patient with severe anemia may appear as what density on CT?
- Acute extra-axial hemorrhage (subarachnoid, epidural, or subdural in location) is usually hyperattenuating when imaged by CT; however, blood must clot in order to be hyperattenuating.
- Hyperacute unclotted blood (and clotted blood in a patient with severe anemia) may be close to water attenuation on CT.
What is the most common cause of subarachnoid hemorrhage?
Where does this SAH tend to occur?
What is the second most common cause?
- Trauma is the most common cause of subarachnoid hemorrhage (SAH), while aneurysm rupture is the most common cause of non-traumatic SAH.
- Traumatic SAH tends to occur contralateral to the side of direct impact, most often in the superficial cerebral sulci.
Epidural Hematomas
What is an arterial epidural hematoma? Classic cause?
What shape do these form? Does it cross cranial sutures?
What is the swirl sign? What density is low attenuation blood?
What would make these a surgical emergency? What can you do if they are small?
Prevalence of venous epidural hematomas? What would these be due to and where and whom do they occur in?
- An arterial epidural hematoma is an extra-axial collection of blood external to the dura, classically caused by fracture of the squamous portion of the temporal bone and resultant tearing of the middle meningeal artery.
- An arterial epidural hematoma has a lentiform shape and does not cross the cranial sutures, where the dura is tightly adherent to the cranium.
- The swirl sign describes mixed high and low attenuation blood within the hematoma and suggests active bleeding. The low attenuation blood is hyperacute unclotted blood while the high attenuation blood is already clotted.
- A large epidural hematoma is a surgical emergency due to mass effect and risk of herniation, although small epidural hematomas can be conservatively managed with serial imaging.
- Venous epidural hematomas are far less common than arterial epidurals and are due to laceration of the dural sinuses, usually occurring in the posterior fossa in children.
Intraventricular Hemorrhage
How can these occur?
Patients with IVH are at an increased risk of what and why?
- Intraventricular hemorrhage can occur due to tearing of subependymal veins or from direct extension of subarachnoid or intraparenchymal hematoma.
- Patients with intraventricular hemorrhage are at increased risk of developing noncommunicating hydrocephalus due to ependymal scarring, which may obstruct the cerebral aqueduct.
What does the coup/countrecoup mechanism describe?
- The coup/contrecoup mechanism of brain trauma describes the propensity for brain to be injured both at the initial site of impact and 180 degrees opposite the impact site, due to secondary impaction against the cranial vault.
What are cortical contusions?
What part of brain do they affect?
A subacute cortical contusion may demonstrate what imaging finding?
How does a chronic contusion appear on CT? How about on MRI?
- A cortical contusion is caused by traumatic contact of the cortical surface of the brain against the rough inner table of the skull.
- Contusions affect the gyral crests and can occur in a coup or a contrecoup location.
- A subacute cortical contusion may demonstrate ring enhancement and should be considered in the differential of a ring-enhancing lesion if there is a history of trauma. Enhancement may continue into the chronic stage.
- A chronic contusion appears as encephalomalacia on CT. MRI is more specific, showing peripheral hemosiderin deposition as hypointense on T2-weighted images and blooming artifact on gradient echo sequences.
Traumatic intraparenchymal hematomas can occur where?
If they occur deeper in the brain, what is the cause?
Similar to cortical contusions, a subacute intraparenchymal hematoma may show what imaging finding?
- Traumatic intraparenchymal hematoma can occur in various locations, ranging from cortical contusion to basal ganglia hemorrhage (due to shearing of lenticulostriate vessels).
- Similar to a cortical contusion, a subacute intraparenchymal hematoma may show ring enhancement.
Diffuse/Traumatic Axonal Injury
What does it result from and what is it caused by?
Most common locations of DAI?
Grading of DIA? Prognosis?
CT appearance?
MR appearance?
- Diffuse/Traumatic axonal injury - DIA is the result of a shear-strain deformation of the brain.
- DAI is caused by rotational deceleration and subsequent reacceleration force that exceeds the limited elastic capacity of the axons.
- The most common locations of DAI include the gray-whiteematter junction, the corpus callosum, and the dorsolateral midbrain. The higher the grade, the worse the prognosis.
- Grade I DAI involves only the gray-white matter junctions.
- Grade II DAI involves the corpus callosum.
- Grade III (most severe) DAI involves the dorsolateral midbrain.
- CT is relatively insensitive for detection of DAI, although hemorrhagic DAI may show tiny foci of high attenuation in the affected regions.
- MRI is much more sensitive to detect DAI, although detection relies on multiple sequences, including FLAIR, GRE, and DWI.
- GRE is extremely sensitive for hemorrhagic axonal injury; however, not all DAI is hemorrhagic.
- FLAIR is most sensitive for nonhemorrhagic DAI.
- Diffusion sequences show restricted diffusion in acute DAI due to cytotoxic edema and cell swelling.
Zygomaticomaxillary Complex Fractures
What is the common name for this fracture? What does this fracture cause?
What does the zygoma normally articulate with via what articulations?
ZMC fxs cause disruption of these articulations by fractures through which structures?
- Commonly but, incorrectly known as the tripod fracture, a zygomaticomaxillary complex (ZMC) fracture causes a floating zygoma by disrupting all four of the zygomatic articulations.
- The zygoma normally articulates with the frontal, maxillary, temporal, and sphenoid bones via the zygomaticofrontal, zygomaticomaxillary, zygomaticotemporal, and zygomaticosphenoid articulations.
- A ZMC fracture causes disruption of the zygomatic articulations by fractures through the following structures:
- Lateral orbital rim fracture: Zygomaticofrontal disruption.
- Inferior orbital rim fracture: Zygomaticomaxillary disruption.
- Zygomatic arch fracture: Zygomaticotemporal disruption.
- Lateral orbital wall: Zygomaticosphenoid disruption.
Le Fort Fractures
What does the Le Fort classification describe? All disrupt what buttress and cause detachment of what bone from skull base?
All Le Fort fractures are defined by fractures through what?
Describe each type of Le Fort fractures (fracture lines through what and resulting free movement of which structures?).
- The Le Fort classification describes a predictable pattern of midface fractures, all of which disrupt the pterygomaxillary buttress and cause detachment of the maxilla from the skull base. All Le Fort fractures are defined by fractures through the pterygoid plates.
- Le Fort I (floating palate) detaches the maxillary alveolus from the skull base.
- Le Fort II dissociates the central midface from the skull, causing the nose and hard palate to be moved as a single unit.
- Le Fort III represents a complete midface dissociation.
Subarachnoid Hemorrhage
Most common causes? In what percent of cases is no cause identified?
How does SAH clinically present?
Initial imaging modality? Appearance?
What other things may also have this imaging appearance?
How sensitive is this initial imaging modality? What should you do if its negative in a suspected case of SAH?
What’s the gold standard for evaluating the presence of an aneurysm?
MR appearance?
- Overall, the most common cause of subarachnoid hemorrhage - SAH is trauma. Aneurysm rupture is by far the most common cause of non-traumatic subarachnoid hemorrhage. No cause of the subarachnoid hemorrhage is identified in up to 22% of cases.
- Clinically, non-traumatic subarachnoid hemorrhage presents with a thunderclap headache and meningismus.
- Noncontrast CT is the initial imaging modality in suspected subarachnoid hemorrhage. On CT, subarachnoid blood appears as high attenuation within the subarachnoid space.
- High attenuation material in the subarachnoid space may be due to SAH (by far the most common cause), meningitis, leptomeningeal carcinomatosis, or prior intrathecal contrast administration.
- Noncontrast CT is >95% sensitive for detecting subarachnoid hemorrhage within the first six hours, with sensitivity slowly decreasing to 50% by day 5. If clinical suspicion for subarachnoid hemorrhage is high with a negative CT scan, the standard of care is to perform a lumbar puncture to look for xanthochromia.
- If SAH is present on imaging or lumbar puncture shows xanthochromia, catheter angiography is the gold standard to evaluate for the presence of an aneurysm. Several recent studies have shown, however, that CT angiography is equivalent to catheter angiography in the search for a culprit aneurysm in cases of SAH.
- On MRI, acute subarachnoid hemorrhage appears hyperintense on FLAIR and demonstrates susceptibility artifact on gradient sequences.
DDx for increased FLAIR signal in the subarachnoid space
This is similar to the DDx for what other imaging?
- The differential diagnosis for increased FLAIR signal in the subarachnoid space is similar to the differential for high attenuation subarachnoid material seen on CT, including:
- SAH
- Meningitis
- Leptomeningeal carcinomatosis
- Residual contrast material.
- Note that meningitis and carcinomatosis will typically show leptomeningeal enhancement in addition to the abnormal FLAIR signal.
- Recent oxygen or propofol administration will also cause increased subarachnoid FLAIR signal.
Distribution of SAH
Multiple aneurysms are seen in up to what percent of patients with SAH?
Subarachnoid blood may redistribute if patients present in what way?
Provide what percent of intracranial aneurysms and in what cystern SAH is found in each below:
- ACOM aneurysm
- PCOM aneurysm
- What else can result from a PCOM aneurysm?
- MCA aneurysm
- Basilar tip aneurysm
- What else may appear like a basilar type aneurysm?
- The pattern of subarachnoid hemorrhage may provide a clue to the location of the ruptured aneurysm. However, multiple aneurysms are seen in up to 20% of patients with SAH, and subarachnoid blood may redistribute if the patient was found down.
- Hemorrhage in the anterior interhemispheric fissure suggests an anterior communicating artery aneurysm (33% of intracranial aneurysms).
- Hemorrhage in the suprasellar cistern suggests a posterior communicating artery aneurysm (also 33% of intracranial aneurysms). Rarely, P-comm aneurysm rupture can result in isolated subdural hemorrhage.
- Hemorrhage in the Sylvian fissure suggests a middle cerebral artery aneurysm (20% of intracranial aneurysms).
- Hemorrhage in the perimesencephalic cistern suggests either a basilar tip aneurysm (5% of intracranial aneurysms), which has a high morbidity, or the relatively benign nonaneurysmal perimesencephalic _subarachnoid hemorrhag_e
Grading of SAH
What are the grading scores?
What are they based on?
Describe the grading criteria.
- The Hunt and Hess score is the clinical grading scale for aneurysmal subarachnoid hemorrhage and is based solely on symptoms, without imaging. Grade I is the lowest grade, with only a mild headache. Grade V is the most severe, with coma or extensor posturing.
- The Fisher grade classifies the CT appearance of SAH. Grade 1 is negative on CT; grades 2 and 3 are <1 mm thick and >1 mm thick, respectively, and grade 4 is diffuse SAH or intraventricular or parenchymal extension.
What is the most common cause of morbidity and mortality in patients who survive the initial episode of SAH?
The peak incidence of this complication?
What can this complication lead to?
Medical treatment? Endovascular treatment?
What other complication can develop in 20-30% of patients, which is due to what? Treatment?
- Vasospasm is the most common cause of morbidity and mortality in patients who survive the initial episode of subarachnoid hemorrhage. The peak incidence of vasospasm occurs approximately 7 days after the initial ictus.
- Vasospasm may lead to stroke or hemorrhage.
- The medical treatment of vasospasm is triple-H therapy of hypertension, hypervolemia, and hemodilution.
- Endovascular treatment of vasospasm involves intra-arterial infusion of vasodilators.
- Approximately 20-30% of patients with subarachnoid hemorrhage will develop acute hydrocephalus, due to obstruction of arachnoid granulations. Treatment is ventriculostomy.
Superficial Siderosis
What is it and what is it due to?
Clinical picture?
Imaging appearance?
Imaging workup?
- Superficial siderosis is a condition caused by iron overload of pial membranes due to chronic or repeated subarachnoid bleeding.
- Clinically, patients with superficial siderosis present with sensorineural deafness and ataxia.
- On imaging, the iron causes hypointensity on T2-weighted images outlining the affected sulci.
- Imaging workup includes cranial and spinal imaging to evaluate for a source of bleeding.
Perimesencephalic SAH
What is this? Prognosis?
The hemorrhage must be limited to where and what is the standard of care?
What is this thought to be a cause of?
Clinical presentation? Prognosis?
- Perimesencephalic subarachnoid hemorrhage is a type of nonaneurysmal subarachnoid hemorrhage that is a diagnosis of exclusion with a much better prognosis than hemorrhage due to a ruptured aneurysm.
- The hemorrhage must be limited to the cisterns directly anterior to the midbrain. The standard of care is to perform catheter angiography twice, one week apart. Both angiograms must be negative. Although the cause of the hemorrhage is unknown, it is thought to represent angiographically occult venous bleeding.
- Although the clinical presentation of perimesencephalic subarachnoid hemorrhage is similar to aneurysmal SAH (__thunderclap headache), patients generally do well without residual neurological deficits. Some patients may experience mild to moderate vasospasm.
Cerebral Venous Anatomy
Name and describe the significance of everything!
What are the dural sinuses?
What are the deep cerebral veins?
What is the venous angle?
What are the superficial cerebral veins?
- Dural sinuses:
- The superior sagittal sinus (and its tributaries) drains the motor and sensory strips.
- The paired transverse sinuses are usually asymmetric, with the left transverse sinus often hypoplastic.
- The sigmoid sinus connects to the jugular bulb.
- The torcular Herophili is the confluence of the superior sagittal sinus, the transverse sinus, and the straight sinus.
- Deep cerebral veins
- The deep cerebral veins consist of the paired internal cerebral veins, the basal vein of Rosenthal, and the vein of Galen.
- The venous angle (red dot in the diagram) is the intersection of the septal vein and the thalamostriate veins. The venous angle is the angiographic landmark for the foramen of Monro.
- Superficial cerebral veins
- The vein of Trolard connects superficial cortical veins to the superior sagittal sinus.
- The vein of Labbé drains the temporal convexity into the transverse or sigmoid sinus.
- Retraction injury to the vein of Labbé during surgery may lead to venous infarction and aphasia.
Venous Thrombosis
What can this lead to in younger patients?
Risk factors?
What is a clue to the diagnosis of venous thrombosis on NCCT? What is the empty delta sign?
MR venogram appearance?
What does venous thrombosis lead to?
- Thrombosis of a cortical vein or a deep venous sinus is one of the more common causes of stroke in younger patients.
- Risk factors for venous thrombosis include pregnancy, oral contraceptives, thrombophilia, malignancy, and infection.
- A clue to the diagnosis of venous thrombosis on NCCT is increased density within the thrombosed sinus or cortical vein (the cord sign). On contrast-enhanced CT, the empty delta sign signifies a filling defect in the superior sagittal sinus.
- MR venogram will show a lack of flow in the thrombosed vein or dural venous sinus.
- Venous thrombosis leads to venous hypertension, which may cause infarction and parenchymal hemorrhage. There are three characteristic patterns of venous infarction, dependent on the location of the thrombosed vein:
- Superior sagittal sinus thrombosis -> infarction of the parasagittal high convexity cortex.
- Deep venous system thrombosis -> infarction of the bilateral thalami.
- Transverse sinus thrombosis -> infarction of the posterior temporal lobe.
What are the specific stages of parenchymal hematoma on MR?
Describe the physiologic stages and timing of iron in Hb and the resultant T1w and T2w appearances!
- Hyperacute hematoma (<6 hours): Intracellular oxyhemoglobin
- Acute hematoma (6–72 hours): Intracellular deoxyhemoglobin
- Early subacute hematoma (3 days to 1 week): Intracellular methemoglobin
- Late subacute hematoma (1 week to months): Extracellular methemoglobin (after RBC lysis)
- Chronic sequela of hemorrhage: Hemosiderin and ferritin
- Remember the bolds and fill in the gaps
Name all the intraparenchymal hemorrhage etiologies and specific clues for each!
- Hypertensive
- Amyloid angiopathy
- Aneurysmal hemorrhage
- AVM
- dAVF
- Cavernous malformation
- Venous thrombosis
- Hemorrhagic neoplasm
- Hemorrhagic infarct
- CNS vasculitis
- Moyamoya
Hypertensive Intraparenchymal Hemorrhage
Prevalence of this type of hemorrhage for spontaneous adult intraparenchymal hemorrhage?
This is due to what?
Etiology?
Characteristic locations?
In addition to location, what other imaging findings suggest this type of bleed?
What other additional findings on GRE or SWI can one detect?
- Chronic hypertension is the most common cause of spontaneous adult intraparenchymal hemorrhage and is due to the secondary microangiopathic effects of chronic hypertension.
- Chronic hypertension causes arteriolar smooth muscle hyperplasia, which eventually leads to smooth muscle death and replacement with collagen. The resultant vascular ectasia predisposes to hemorrhage.
- Hypertensive hemorrhage occurs in characteristic locations in the basal ganglia, thalamus, and cerebellum.
- In addition to location, imaging (MRI or CT) findings suggestive of a hypertensive bleed include additional stigmata of hypertensive microangiopathy, such as periventricular white matter disease and prior lacunar infarcts.
- An additional MR-specific finding suggesting hypertensive hemorrhage is the presence of microhemorrhages on T2* (GRE or SWI) in the basal ganglia or brainstem.
